Mel Eckersley-Maslin

Mel Eckersley-Maslin

@meleckmas.bsky.social

Lab head in stem cell and cancer epigenetics at PeterMac, UniMelb 🇦🇺🧬 Scientist, mum, dreamer She/her. Views are my own www.eckmaslab.com

1.2K followers867 following68 posts

I had fun chatting with Stefan on this Epigenetics podcast, thanks for the invitation!

Epigenetics Podcast@epigeneticspod.bsky.social

In this episode of the Epigenetics Podcast, we talked with @meleckmas.bsky.social from the Peter McCallum Cancer Center about her work on DPPA2 and DPPA4 as Chromatin Priming Factors. #podcast #epigenetics Listen here: activemotif.com/podcasts-mel...

Mel Eckersley-Maslin reposted

Thrilled to share my freshly "baked" Baker lab paper. We took a bottom-up approach to designing transcriptional regulators. Instead of relying on natural activation domains, we designed compact proteins that recruit specific cofactors. Activators for now, repressors to come!

Had a great time last week at the #CancerEpigenetics meeting in Paris where I had the opportunity to share our latest work on bivalent chromatin dynamics in cancer. Thanks Pierre-Antoine Defossez for organising and ensuring the conference success despite all the protests!

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Interestingly, similarity to the trophectoderm, the precursor to the placenta, is highly detrimental for skin and breast cancers. This tumour intrinsic property is independent of known clinical and molecular attributes, and can predict dependencies to several key preclinical targets including MYBL2

Whilst all cancers upregulate early embryonic programs, the impact on patient survival is context dependent. Surprisingly, similarity to maternal stage embryos is protective in kidney cancer. Further analysis revealed this signal comes form the stroma, not the tumour, in response to the cancer cells

Mel Eckersley-Maslin reposted

1\ We know a bit about how 3D chromatin interactions are formed, but what do we know about how they are disrupted? We asked this question in our latest preprint: doi.org/10.64898/202..., focusing on the massive loss of promoter interactions during neuronal differentiation.

doi.orgDevelopmentally programmed loss of long-range Polycomb interactions is regulated by cohesinDistal regulatory elements (DREs), such as enhancers, can regulate genes across megabase-long distances, presumably via coming into close spatial proximity. The establishment of new transcriptional programmes during cell type transitions is associated with widespread rewiring of the spatial organisation of the genome, including gain and loss of chromatin interactions. Extensive effort has been invested into understanding how chromatin interactions are formed during development, yet the mechanisms underlying their developmental loss remain largely unclear. By leveraging chromatin accessibility-assisted footprinting, acute protein degradation and chromatin conformation capture, we show that loss of promoter interactions cannot be explained by reduced binding of sequence-specific transcription factors (TFs). Instead, we identify a subset of interactions that depend on cohesin for programmed developmental disruption. These sites are characterized by high Polycomb enrichment and TF occupancy and engage in strong long-range interactions that undergo extensive differentiation-dependent rewiring. Preventing interaction loss by acute cohesin degradation results in the preferential downregulation of associated genes. Together, these results suggest that cohesin indirectly regulates developmental loss of Polycomb interactions by enabling the acquisition of other potentially regulatory contacts in a process that may shape transcriptional programs during cell type transitions. ### Competing Interest Statement The authors have declared no competing interest. European Research Council Helmholtz Society, VH-NG-1604

Sad to hear about Terri’s passing. I have fond memories of her from my graduate student days at CSHL. and am grateful for some rather direct career advice she gave me at the time. My thoughts are with all those close to her. She will be missed

Richard Sever@richardsever.bsky.social

Deeply saddened to learn of the death of my colleague Terri Grodzicker. She was an amazing molecular biologist who did fundamental work on adenovirus. Many will know her as the charismatic long-time editor of Genes & Development and organizer of CSHL meetings 1/2 en.wikipedia.org/wiki/Terri_G...

Mel Eckersley-Maslin reposted

🚨 #Postdoc position open. Want to understand non-canonical #epigenetic regulation of mammalian transcription? Come work @uoe-igc.bsky.social in Edinburgh! We’re looking for a motivated & collaborative colleague with a strong track record. 📅 14 October 2026 📢 Please share Apply here 👇

elxw.fa.em3.oraclecloud.comPost-Doctoral Research AssociateAn exciting postdoctoral position is available to research the role of epigenetic marks in gene regulation.

Mel Eckersley-Maslin reposted

Reposting this ongoing search (any discipline of biology) for an Assistant to Associate level colleague in the Division of Basic Sciences at Fred Hutch. Great city, great colleagues, great core facilities, great trainees.

Harmit Singh Malik@harmitmalik.bsky.social

Come be our colleague. I have been in this Division for 27 years (4 as a postdoc and 23 as a PI). It is an amazing place to work, collaborate, and be inspired. If you are applying to be an Assistant or Associate Professor this Fall, don't miss this deadline.

Our lab had an international brunch where everyone brought in something from their culture to share. They even printed out little place-cards with flags and ingredients. So much delicious food!

Intestinal stem cells count divisions and Polycomb/trithorax proteins are involved in the counting, implicating chromatin control. Love the model but would be great to know if it’s truely counting and not time, and how mechanistically replication dilution of histone mods ensures 9 cell cycles?

Mel Eckersley-Maslin reposted

New paper 🧵 What if the "landscape" that guides cell differentiation isn't fixed, but is sculpted, in real time, by the very cells moving through it? We call this a 'sandscape' : grains of sand that carve dunes as they move, while the dunes' shape simultaneously steers where the grains go next.

Mel Eckersley-Maslin reposted

Mel Eckersley-Maslin reposted

We just started our summer break, but we're also planning our September-December seminar schedule! If you have an exciting chromatin/transcription story that will be ready for the spotlight by then, use the survey below to nominate yourself to give a #FNucleosome talk 🧬🧬 forms.gle/1EKYN2Nt79ar...

forms.gleApplication to speak in the Fragile Nucleosome seriesThank you for your interest in our seminar series! We use a variety of different session formats but, in general, trainees can plan for a ~15 min talk + 5min Q/A and PIs can plan for a ~25min talk +...

Mel Eckersley-Maslin reposted

📢 We are looking for a Junior Group Leader to join us at @institutcurie.bsky.social! Having joined the department just over a year ago, I can honestly say that it is an exceptionally stimulating and supportive scientific environment, filled with outstanding colleagues — all in the heart of Paris.

Mel Eckersley-Maslin reposted

Exciting breakthrough technology from the lab, now live in @cellcellpress.bsky.social ! Instead of cutting the genome where proteins bind (e.g., Cut&Tag), D&D-seq scars the DNA with a deaminase, allowing single cell genome mapping of TFs and chromatin remodellers!

Mel Eckersley-Maslin reposted

𝗔𝗽𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀 𝗮𝗿𝗲 𝗻𝗼𝘄 𝗼𝗽𝗲𝗻 𝗳𝗼𝗿 𝘁𝗵𝗲: 𝗔𝗘𝗽𝗶𝗔 𝗦𝘂𝘀𝗮𝗻 𝗖𝗹𝗮𝗿𝗸 𝗔𝘄𝗮𝗿𝗱 𝗳𝗼𝗿 𝗥𝗲𝘀𝗲𝗮𝗿𝗰𝗵 𝗘𝘅𝗰𝗲𝗹𝗹𝗲𝗻𝗰𝗲 @aepia.bsky.social is excited to open applications for the Susan Clark Award for Research Excellence, recognising outstanding contributions in epigenetics research, leadership, and advocacy.

If we introduce DPPA2/4 in non-small cell lung cancer cells where it's not usually expressed, it binds active CpG rich regions. Here it changes the chromatin states at over half its binding sites to a more active state (as determined by ChromHMM) (7/8)

PRC2 is at these sites, but not it's product H3K27me3. We noticed H3K27ac was also there so hypothesised it might be blocking PRC2 activity. However removing H3K27ac (using A-485), at least for 24hrs, did not lead to an increase in H3K27me3 (5/8)

What happens if DPPA2/4 is removed? Surprisingly, the classic bivalent marks it regulates in stem cells (H3K4me3 and H3K27me3) are unaltered. Neither is transcription or chromatin accessibility. Instead we see a loss of H2AK119ub at these unique active sites (6/8)

Co-expression of Developmental Pluripotency Associated 2 and 4 (DPPA2/4) is linked with worse survival, in particular for non-small cell lung cancer. So we generated a series of knockdown, over-expression and knockout cell models to understand molecularly why this is (2/8)

Mel Eckersley-Maslin reposted